Inhibition provided by local GABAergic interneurons (INs) activates ionotropic GABA A and metabotropic GABA B receptors (GABA B Rs). Despite GABA B Rs representing a major source of inhibition, little is known of their function in distinct IN subtypes. Here, we show that, while the archetypal dendritic-inhibitory somatostatin-expressing INs (SOM-INs) possess high levels of GABA B R on their somato-dendritic surface, they fail to produce significant postsynaptic inhibitory currents. Instead, GABA B Rs selectively inhibit dendritic Ca V 1.2 (L-type) Ca 2+ channels on SOM-IN dendrites, leading to reduced calcium influx and loss of long-term potentiation at excitatory input synapses onto these INs. These data provide a mechanism by which GABA B Rs can contribute to disinhibition and control the efficacy of extrinsic inputs to hippocampal networks. Booker et al. show that GABA B receptors are highly expressed on somatostatin interneuron dendrites. Rather than activating Kir3 channels, they preferentially co-cluster with, and negatively couple to, L-type calcium channels inhibiting long-term potentiation at excitatory inputs.
Booker, S. A., Loreth, D., Gee, A. L., Watanabe, M., Kind, P. C., Wyllie, D. J. A., … Vida, I. (2018). Postsynaptic GABA B Rs Inhibit L-Type Calcium Channels and Abolish Long-Term Potentiation in Hippocampal Somatostatin Interneurons. Cell Reports, 22(1), 36–43. https://doi.org/10.1016/j.celrep.2017.12.021